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Suppressor of cytokine signaling 3 (SOCS3) is related to pro-inflammatory cytokine production and triglyceride deposition in turbot (Scophthalmus maximus)
Tan, P.; Peng, M.; Liu, D.; Guo, H.; Mai, K.; Nian, R.; Macq, B.; Ai, Q. (2017). Suppressor of cytokine signaling 3 (SOCS3) is related to pro-inflammatory cytokine production and triglyceride deposition in turbot (Scophthalmus maximus). Fish Shellfish Immunol. 70: 381-390. https://hdl.handle.net/10.1016/j.fsi.2017.09.006
In: Fish & Shellfish Immunology. Academic Press: London; New York. ISSN 1050-4648; e-ISSN 1095-9947, more
Peer reviewed article  

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Keyword
    Marine
Author keywords
    High-lipid diet; Suppressor of cytokine signaling 3; Toll-likereceptor-nuclear transcription factor kappa-B; Triglyceride; Maturesterol regulatory element binding protein 1

Authors  Top 
  • Tan, P.
  • Peng, M.
  • Liu, D.
  • Guo, H.
  • Mai, K.
  • Nian, R.
  • Macq, B., more
  • Ai, Q.

Abstract
    Turbot (Scophthalmus maximus) is an economically important fish that is farmed by aquaculture for human consumption. Aquacultured turbot are commonly fed a high-lipid diet; however, this diet causes excessive lipid deposition and the overexpression of pro-inflammatory cytokines. Studies in mammals have indicated that a relationship exists between pro-inflammatory cytokine overexpression and altered lipid metabolism through the activation of suppressor of cytokine signaling 3 (SOCS3). In this study, we investigated the relationship between SOCS3 and triglyceride (TG) deposition and mechanism of SOCS3 activation in farmed turbot fed high-lipid diet (HLD). TG content increased with SOCS3 production, mediated by toll-like receptor-nuclear transcription factor kappa-B (TLR-NFκB) signaling in the liver of turbot fed a HLD and in turbot primary liver cells incubated with oleic acid (OA). Overexpression of SOCS3 increased TG deposition via the increased production of mature sterol regulatory element binding protein 1 (m-SREBP-1). Knockdown of SOCS3 in turbot primary liver cells resulted in normalized TG deposition and decreased m-SREBP-1 production. These results suggest that the HLD and OA can induce cytokine expression by activating the TLR-NFκB signaling pathways, resulting in increased SOCS3 expression. It is proposed that SOCS3 enhances m-SREBP-1 production, leading to TG deposition. These findings provide important new insights into the relationship between cytokine expression and TG deposition and mechanism of HLD-induced pro-inflammatory response, which could help to improve the health of farmed turbot and a better understanding of fish immunity.

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